Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2007-10-3
pubmed:abstractText
Innate immune cells may regulate adaptive immunity by balancing different lineages of T cells and providing negative costimulation. In addition, CD11b(+)Gr-1(+) myeloid-derived suppressor cells have been described in tumor, parasite infection, and severe trauma models. In this study, we observe that splenic CD11b(+) cells markedly increase after experimental autoimmune encephalomyelitis (EAE) immunization, and they suppress T cell proliferation in vitro. Although >80% of CD11b(+) cells express varying levels of Gr-1, only a small population of CD11b(+)Ly-6C(high) inflammatory monocytes (IMC) can efficiently suppress T cell proliferation and induce T cell apoptosis through the production of NO. IFN-gamma produced by activated T cells is essential to induce IMC suppressive function. EAE immunization increases the frequencies of IMC in the bone marrow, spleen, and blood, but not in the lymph nodes. At the peak of EAE, IMC represent approximately 30% of inflammatory cells in the CNS. IMC express F4/80 and CD93 but not CD31, suggesting that they are immature monocytes. Furthermore, IMC have the plasticity to up-regulate NO synthase 2 or arginase 1 expression upon different cytokine treatments. These findings indicate that CD11b(+)Ly-6C(high) IMC induced during EAE priming are powerful suppressors of activated T cells. Further understanding of suppressive monocytes in autoimmune disease models may have important clinical implications for human autoimmune diseases.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
179
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5228-37
pubmed:meshHeading
pubmed-meshheading:17911608-Amino Acid Sequence, pubmed-meshheading:17911608-Animals, pubmed-meshheading:17911608-Antigens, CD11b, pubmed-meshheading:17911608-Antigens, Ly, pubmed-meshheading:17911608-Apoptosis, pubmed-meshheading:17911608-Cell Differentiation, pubmed-meshheading:17911608-Cell Proliferation, pubmed-meshheading:17911608-Cells, Cultured, pubmed-meshheading:17911608-Encephalomyelitis, Autoimmune, Experimental, pubmed-meshheading:17911608-Female, pubmed-meshheading:17911608-Immunophenotyping, pubmed-meshheading:17911608-Immunosuppression, pubmed-meshheading:17911608-Mice, pubmed-meshheading:17911608-Mice, Inbred BALB C, pubmed-meshheading:17911608-Mice, Inbred C57BL, pubmed-meshheading:17911608-Mice, Transgenic, pubmed-meshheading:17911608-Molecular Sequence Data, pubmed-meshheading:17911608-Monocytes, pubmed-meshheading:17911608-Spleen, pubmed-meshheading:17911608-T-Lymphocyte Subsets
pubmed:year
2007
pubmed:articleTitle
CD11b+Ly-6C(hi) suppressive monocytes in experimental autoimmune encephalomyelitis.
pubmed:affiliation
Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural